论文部分内容阅读
目的:探讨氯吡格雷对不稳定型心绞痛(ACS)患者血浆炎症因子和血小板活化因子的影响。方法:70例ACS患者随机分为两组,均按ACS治疗方案进行治疗,观察组在此基础上加用氯吡格雷75 mg,po,qd,连用8周。观察两组患者治疗前后血浆炎症因子hs-CRP、TNF-α、IL-6水平和血小板活化因子CD62p、CD63水平的变化。结果:两组患者治疗前血浆hs-CRP、IL-6和TNF-α水平比较,差异无统计学意义(P>0.05)。治疗8周后,两组患者血浆hs-CRP、IL-6和TNF-α水平均较治疗前明显下降(P<0.05或0.01),且观察组下降的幅度较对照组更明显(P<0.05)。两组患者治疗前血浆血小板活化因子CD62p和CD63水平差异无统计学意义(P>0.05),治疗8周后,两组患者血浆CD62p和CD63水平均较治疗前明显下降(P<0.05或0.01),且观察组下降的幅度较对照组更明显(P<0.05)。结论:氯吡格雷对ACS患者具有抗炎,抑制血小板活化作用,从而改善血管内斑块的炎症反应,减少血小板的黏附和聚集作用,在一定程度上增加动脉粥样斑块的稳定性、阻断和逆转冠状动脉粥样斑块作用。
Objective: To investigate the effect of clopidogrel on plasma inflammatory factors and platelet activating factor in patients with unstable angina pectoris (ACS). Methods: Seventy ACS patients were randomly divided into two groups and were treated by ACS. The observation group was given Clopidogrel 75 mg, po, qd for 8 weeks. The changes of plasma inflammatory cytokines such as hs-CRP, TNF-α, IL-6 and platelet-activating factor CD62p and CD63 before and after treatment were observed. Results: There was no significant difference in plasma hs-CRP, IL-6 and TNF-α levels between the two groups before treatment (P> 0.05). After 8 weeks of treatment, the levels of plasma hs-CRP, IL-6 and TNF-α in the two groups were significantly lower than those before treatment (P <0.05 or 0.01), and the decrease in the observation group was more significant than that in the control group (P <0.05 ). The plasma levels of CD62p and CD63 before treatment did not show significant difference between the two groups (P> 0.05). After 8 weeks of treatment, the plasma levels of CD62p and CD63 in both groups were significantly lower than those before treatment (P <0.05 or 0.01) , And the observation group decreased more significantly than the control group (P <0.05). CONCLUSION: Clopidogrel has anti-inflammatory and anti-inflammatory effects on patients with ACS, thereby improving the inflammatory reaction of intravascular plaque, reducing platelet adhesion and aggregation, and increasing the stability of atherosclerotic plaque to a certain extent Broke and reverse coronary atherosclerotic plaque.